Oral Recombinant Methioninase Inhibits Diabetes Onset in Mice on a High-fat Diet.
Animals
Biomarkers
Blood Glucose
Carbon-Sulfur Lyases
/ administration & dosage
Diabetes Mellitus, Experimental
/ drug therapy
Diet, High-Fat
/ adverse effects
Disease Models, Animal
Glucose
/ metabolism
Hypoglycemic Agents
/ administration & dosage
Lipids
/ blood
Mice
Recombinant Proteins
/ administration & dosage
MR
Methioninase
diabetes
high-fat diet
methionine restriction
mice
Journal
In vivo (Athens, Greece)
ISSN: 1791-7549
Titre abrégé: In Vivo
Pays: Greece
ID NLM: 8806809
Informations de publication
Date de publication:
Historique:
received:
30
12
2019
revised:
21
01
2020
accepted:
24
01
2020
entrez:
2
5
2020
pubmed:
2
5
2020
medline:
13
2
2021
Statut:
ppublish
Résumé
We have recently shown that oral recombinant methionase (o-rMETase) prevents obesity in mice on a high-fat (HF) diet. The present study aimed to determine if o-rMETase can inhibit the onset of diabetes in mice on a HF diet. The mice on a HF diet were divided into two groups: 1) HF+phosphate buffered saline (PBS) group; 2) HF+o-rMETase group. The blood glucose level in the HF+PBS group increased to average of 201 mg/dl during the experimental period of 8 weeks. In contrast, the blood glucose level in the HF+o-rMETase group maintained an average of 126 mg/dl (p<0.01, HF+PBS vs. HF+o-rMETase). The glucose tolerance test showed a significant increase in tolerance in the HF+o-rMETase group at 120 min after glucose injection compared to the HF+PBS group (p=0.04). Visceral adipose tissue was significantly less in the HF+o-rMETase group than the HF+PBS group (p=0.05). There was no difference in insulin levels, cholesterol or triglycerides between the HF+PBS and HF+o-rMETase groups. o-rMETase inhibited the onset of diabetes as well as prevented obesity on a high-fat diet, offering a possibility of a new and easy-to-use alternative to severe dieting or insulin injections.
Sections du résumé
BACKGROUND/AIM
OBJECTIVE
We have recently shown that oral recombinant methionase (o-rMETase) prevents obesity in mice on a high-fat (HF) diet. The present study aimed to determine if o-rMETase can inhibit the onset of diabetes in mice on a HF diet.
MATERIALS AND METHODS
METHODS
The mice on a HF diet were divided into two groups: 1) HF+phosphate buffered saline (PBS) group; 2) HF+o-rMETase group.
RESULTS
RESULTS
The blood glucose level in the HF+PBS group increased to average of 201 mg/dl during the experimental period of 8 weeks. In contrast, the blood glucose level in the HF+o-rMETase group maintained an average of 126 mg/dl (p<0.01, HF+PBS vs. HF+o-rMETase). The glucose tolerance test showed a significant increase in tolerance in the HF+o-rMETase group at 120 min after glucose injection compared to the HF+PBS group (p=0.04). Visceral adipose tissue was significantly less in the HF+o-rMETase group than the HF+PBS group (p=0.05). There was no difference in insulin levels, cholesterol or triglycerides between the HF+PBS and HF+o-rMETase groups.
CONCLUSION
CONCLUSIONS
o-rMETase inhibited the onset of diabetes as well as prevented obesity on a high-fat diet, offering a possibility of a new and easy-to-use alternative to severe dieting or insulin injections.
Identifiants
pubmed: 32354882
pii: 34/3/973
doi: 10.21873/invivo.11865
pmc: PMC7279799
doi:
Substances chimiques
Biomarkers
0
Blood Glucose
0
Hypoglycemic Agents
0
Lipids
0
Recombinant Proteins
0
Carbon-Sulfur Lyases
EC 4.4.-
L-methionine gamma-lyase
EC 4.4.1.11
Glucose
IY9XDZ35W2
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
973-978Informations de copyright
Copyright© 2020, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.
Références
Cancer Res. 1973 Aug;33(8):1862-5
pubmed: 4720797
PLoS One. 2012;7(12):e51357
pubmed: 23236485
Br J Nutr. 2013 Oct;110(8):1534-47
pubmed: 23591120
J Nutr. 2017 Oct;147(10):1892-1899
pubmed: 28835389
Protein Expr Purif. 1997 Mar;9(2):233-45
pubmed: 9056489
J Laparoendosc Adv Surg Tech A. 2019 May;29(5):655-662
pubmed: 30452318
Obes Rev. 2003 Nov;4(4):257-90
pubmed: 14649376
Surg Obes Relat Dis. 2010 May-Jun;6(3):290-5
pubmed: 20510293
Obes Res. 2005 Nov;13(11):1961-9
pubmed: 16339128
Development. 2013 Oct;140(19):3939-49
pubmed: 24046315
Aging Cell. 2017 Feb;16(1):125-135
pubmed: 27653523
N Engl J Med. 2013 Jul 11;369(2):145-54
pubmed: 23796131
Home Healthc Now. 2016 Sep;34(8):416-23
pubmed: 27580280
Mech Ageing Dev. 2016 Jul;157:35-43
pubmed: 27453066
J Psychosom Res. 1986;30(5):567-73
pubmed: 3772838
Ann Intern Med. 2002 Jul 2;137(1):25-33
pubmed: 12093242
Med Hypotheses. 2009 Feb;72(2):125-8
pubmed: 18789600
Int J Obes (Lond). 2019 Nov;43(11):2217-2224
pubmed: 30696933
Int J Behav Med. 2010 Sep;17(3):176-81
pubmed: 20033629
Ageing Res Rev. 2017 Oct;39:87-95
pubmed: 27570078
In Vivo. 2020 Mar-Apr;34(2):489-494
pubmed: 32111745
Diabetes Res Clin Pract. 2017 Jun;128:40-50
pubmed: 28437734
Diabetes. 2014 Nov;63(11):3721-33
pubmed: 24947368
Obes Surg. 2018 Feb;28(2):497-505
pubmed: 28795271
Int J Obes (Lond). 2005 Jan;29(1):122-8
pubmed: 15545976
Int J Obes (Lond). 2008 Apr;32(4):692-9
pubmed: 18071341
Eur J Clin Nutr. 2016 Mar;70(3):306-12
pubmed: 26395436
Am J Clin Nutr. 2009 May;89(5):1607S-1612S
pubmed: 19321569
Obes Surg. 2008 Jun;18(6):648-51
pubmed: 18392907
Diabetes Res Clin Pract. 2005 Feb;67(2):152-62
pubmed: 15649575
Obes Surg. 2017 May;27(5):1137-1144
pubmed: 27798793
Ann Surg. 2006 Nov;244(5):734-40
pubmed: 17060766
Diabetologia. 1985 Jul;28(7):412-9
pubmed: 3899825